Co-reporter:Aijing Sun, Jieqing Liu, Suqiu Pang, Junsheng Lin, Ruian Xu
Bioorganic & Medicinal Chemistry Letters 2016 Volume 26(Issue 9) pp:2375-2379
Publication Date(Web):1 May 2016
DOI:10.1016/j.bmcl.2016.01.076
7-Hydroxy-2-methoxy-phenanthrene-3,4-dione and 3′,7′,7-trihydroxy-2,2′,4′-trimethoxy-[1,8′-biphenanthrene]-3,4-dione, two novel compounds and four known compounds were isolated from Bletilla striata. The structures of the compounds were established on the basis of extensive spectroscopic analysis. The two compounds exhibited antiproliferative effects using the MTT test; these effects may be due to cell cycle arrest and inducing ROS generation.
Co-reporter:Weihong Qu, Mingxi Wang, Yaqing Wu, Yinghui Lv, Qizhao Wang, Ruian Xu
Journal of Chromatography B 2015 990() pp: 15-22
Publication Date(Web):
DOI:10.1016/j.jchromb.2015.03.003
Co-reporter:Qiuyan Liu;Yu Luo;Xiaotong Li;Li Yuan
Applied Biochemistry and Biotechnology 2013 Volume 169( Issue 8) pp:2273-2280
Publication Date(Web):2013 April
DOI:10.1007/s12010-012-0081-2
Quaking (QKI) proteins are important regulators of RNA metabolism and cellular signal transduction. Recent studies have shown that isoforms of QKI proteins, which include QKI5/6/7/7b in human cells, play important roles in the development of neurological diseases and human cancers. In comparison with QKI5/6/7, however, there are little data on QKI7b due to lack of specific antibodies. Here, we reported the preparation and initial characterizations of polyclonal antibodies against human QKI7b. Utilizing a chemically synthesized C-terminal peptide fragment of human QKI7b, we raised two preparations of rabbit antiserum. We found that these antibodies were able to recognize human QKI7b, but not QKI5/6/7. Our immunofluorescence staining showed that in LO2 hepatocytes, QKI7b localizes predominantly in the perinuclear cytoplasm and less abundantly in the nucleus. In clinical samples, we showed that like QKI5/6/7 proteins, QKI7b protein was also significantly downregulated in most human colorectal cancer tissues. These antibodies, therefore, might be useful in future functional studies of QKI7b.
Co-reporter:Hua Li;Xinyan Li;Karen S. L. Lam;Sidney Tam
Journal of Biomedical Science 2008 Volume 15( Issue 4) pp:487-497
Publication Date(Web):2008 July
DOI:10.1007/s11373-008-9233-3
Inducing autologous liver cells to differentiate into endocrine β cell has been a potential strategy for the treatment of type 1diabetes. However it is still not known which sub-population cells in the liver was responsible for this developmental shift. Pancreatic and duodenal homeobox gene 1 (pdx-1), a crucial transcription factor in pancreatic islet development and differentiation, has attracted much interests in beta cell differentiation experiments. This study was conducted to evaluate whether pdx-1 gene delivered by adeno-associated virus (AAV) could induce autologous liver cells to differentiate into insulin-producing cells and to explore the origin of these cells. Here we used 4 × 10e11 AAV to deliver pdx-1 to STZ-induced diabetic rats via the portal vein. Immunofluorescent staining showed more insulin-positive cells, which had similar morphology with hepatic oval stem cells and were positive for hepatic oval stem cell markers, Thy-1 and cytokeratin 19 (ck19). In addition to the expression of pdx-1, insulin1 and insulin2, RT-PCR and quantitative real-time PCR also detected significantly higher levels of other important transcription factors in AAV-pdx-1 treated diabetic rat livers. AAV-pdx-1 treated diabetic rats showed partially ameliorated hyperglycemia, better gain of body weight and improved lipid levels. Our data indicated that rat hepatic oval stem cells were differentiated into bioactive insulin-producing cells by AAV-pdx-1 delivery in diabetic rats, with promoted expression of some transcription factors necessary for beta cell development and function.
Co-reporter:Zhiyun Cheng, Yinghui Lv, Suqiu Pang, Ruyu Bai, Mingxi Wang, Shuyu Lin, Tianwen Xu, Duncan Spalding, Nagy Habib, Ruian Xu
Acta Pharmaceutica Sinica B (May 2015) Volume 5(Issue 3) pp:194-200
Publication Date(Web):May 2015
DOI:10.1016/j.apsb.2015.02.003